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Muscarinic M1, M3, Nicotinic,GABAA and GABAB Receptor ...

Muscarinic M1, M3, Nicotinic,GABAA and GABAB Receptor ...

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120<br />

Discussion<br />

al., 1992), it has the ability to affect neuronal migration (Komuro & Rakic, 1996)<br />

as well as other developmental functions such as apoptosis (Sastry & Rao, 2000).<br />

In the present study, the up regulation of α7 nicotinic receptor is<br />

associated with altered <strong>and</strong> hypofunction of the receptor induced by glucose<br />

deprivation during hypoglycemia <strong>and</strong> diabetes which also leads to cognitive <strong>and</strong><br />

memory deficits. <strong>Nicotinic</strong> receptor activation has been reported to improve<br />

performance in tests measuring several forms of learning <strong>and</strong> memory <strong>and</strong> its<br />

effects appear to be most robust for working memory (Levin 1992; Levin &<br />

Simon 1998). Present findings showed that the behavioural anomalities observed<br />

in glucose deprived /hypoglycemic rats are attributed to impaired function of α7<br />

nicotinic receptors. These receptors mediate fast synaptic transmission (Alkondon<br />

et al., 1998; Frazier et al., 1998; Chang & Berg, 1999) <strong>and</strong> modulation of synaptic<br />

transmission mediated by transmitters such as acetylcholine, dopamine, glutamate,<br />

gamma aminobutyric acid (GABA) (MacDermott et al., 1999) norepinephrine <strong>and</strong><br />

<strong>and</strong> serotonin which is altered by recurrent hypoglycemic attacks in diabetic <strong>and</strong><br />

non-diabetic rats.<br />

CENTRAL GABA RECEPTOR ALTERATIONS IN EXPERIMENTAL<br />

RATS<br />

Symptoms associated with hypoglycemic are related to the release of<br />

catecholamines, however, at times, transient neurological deficits, presumably<br />

resulting from a low intracerebral glucose concentration, accompany the typical<br />

clinical picture. These transient neurological deficits may be generalized such as<br />

confusion, motor restlessness, hypotonia <strong>and</strong> generalized seizures (Lahat, 1995).<br />

Epileptic episodes induced by hypoglycemia are the cause of neurological deficits<br />

(Wayne et al., 1990). GABA, the major inhibitory neurotransmitter in the CNS<br />

(Sivilotti & Nistri, 1991) plays an important role in seizure generation. Excitatory<br />

<strong>and</strong> inhibitory neurotransmission in the CNS is mediated mainly by glutamate <strong>and</strong><br />

GABA, respectively. A dysfunction of any of these neurotransmitter systems is

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